Overactive bladder is characterized by involuntary contractions of the detrusor muscle during bladder filling, which result in a sudden urge to urinate. The urge may be difficult to suppress, and can lead to involuntary loss of urine. Clinical manifestations of detrusor instability include urinary frequency, urinary urgency, and urinary urge incontinence.
Though little is known about the mechanisms underlying detrusor instability, recent studies suggest that the abnormal activity of the detrusor muscle may be a consequence of changes in the morphology and physiological or biochemical function of nerve, muscle, and connective tissues. These changes likely originate from defects on the cellular level or from changes in the nervous system. See M. J. Drake et al., Model of peripheral autonomous modules and a myovesical plexus in normal and overactive bladder function, 350 The Lancet 401, 401-403 (2001). Morphological studies show that changes to the nerve, muscle, and connective tissues are not uniform in idiopathic and neuropathic bladders. Instead, discrete areas of connective tissue infiltration, muscle hypertrophy, and altered innervations have been observed. See R. G. Charlton et al., Focal changes in nerve, muscle and connective tissue in normal and unstable human bladder, 84 BJU Int. 953, 953-960 (1999). These localized changes in the morphology of bladder tissue may contribute to abnormal function of the detrusor muscle on a macroscopic scale.
Moreover, studies suggest that the abnormal activity of the detrusor muscle may originate from one or more distinct anatomical areas of the bladder. For example, the abnormal activity of the detrusor muscle may originate in either the bladder dome or the internal sphincter, resulting in the dyssynchronous function of the entire bladder. In some instances, abnormal activity of the detrusor muscle may originate in the trigone. Evidence of cellular communication between the trigone and the detrusor muscle suggests that spontaneous activity of the trigone may be a precursor to bladder overactivity. See A. Roosen et al., Characteristics of Spontaneous Activity in the Bladder Trigone, 56 European Urology 346, 346-354 (2009).
Current methods to treat bladder overactivity include systemic drugs, nerve stimulation, and electrical stimulation. These known methods target the function of the entire bladder and do not address local changes and activity originating at specific anatomical areas of the bladder. Therefore, a need exists for methods and systems capable of both identifying and/or delivering therapy to specific anatomical areas of the bladder.